Acute Kidney Injury in COVID-19: The Chinese Experience

Zheng, Xizi; Zhao, Yutong; Li, Yang

doi:10.1016/j.semnephrol.2020.09.001

Cited by 37 publications

(32 citation statements)

References 93 publications

(181 reference statements)

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“…An alarming number of patients also developed acute kidney injury (AKI). Indeed, AKI in patients with COVID-19 infection is reported to range between 6.5% and 46% [ 2 , 3 , 4 , 5 ], with the highest ranges in the critically ill (23%–81%) [ 3 , 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 ]. Differences in the incidence of AKI have resulted from the various definitions of AKI used and the populations studied.…”

Section: Introductionmentioning

confidence: 99%

Severe Acute Kidney Injury in Critically Ill Patients with COVID-19 Admitted to ICU: Incidence, Risk Factors, and Outcomes

Ghosn

Attallah

Badr³

et al. 2021

JCM

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Background: Critically ill patients with COVID-19 are prone to develop severe acute kidney injury (AKI), defined as KDIGO (Kidney Disease Improving Global Outcomes) stages 2 or 3. However, data are limited in these patients. We aimed to report the incidence, risk factors, and prognostic impact of severe AKI in critically ill patients with COVID-19 admitted to the intensive care unit (ICU) for acute respiratory failure. Methods: A retrospective monocenter study including adult patients with laboratory-confirmed severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection admitted to the ICU for acute respiratory failure. The primary outcome was to identify the incidence and risk factors associated with severe AKI (KDIGO stages 2 or 3). Results: Overall, 110 COVID-19 patients were admitted. Among them, 77 (70%) required invasive mechanical ventilation (IMV), 66 (60%) received vasopressor support, and 9 (8.2%) needed extracorporeal membrane oxygenation (ECMO). Severe AKI occurred in 50 patients (45.4%). In multivariable logistic regression analysis, severe AKI was independently associated with age (odds ratio (OR) = 1.08 (95% CI (confidence interval): 1.03–1.14), p = 0.003), IMV (OR = 33.44 (95% CI: 2.20–507.77), p = 0.011), creatinine level on admission (OR = 1.04 (95% CI: 1.008–1.065), p = 0.012), and ECMO (OR = 11.42 (95% CI: 1.95–66.70), p = 0.007). Inflammatory (interleukin-6, C-reactive protein, and ferritin) or thrombotic (D-dimer and fibrinogen) markers were not associated with severe AKI after adjustment for potential confounders. Severe AKI was independently associated with hospital mortality (OR = 29.73 (95% CI: 4.10–215.77), p = 0.001) and longer hospital length of stay (subhazard ratio = 0.26 (95% CI: 0.14–0.51), p < 0.001). At the time of hospital discharge, 74.1% of patients with severe AKI who were discharged alive from the hospital recovered normal or baseline renal function. Conclusion: Severe AKI was common in critically ill patients with COVID-19 and was not associated with inflammatory or thrombotic markers. Severe AKI was an independent risk factor of hospital mortality and hospital length of stay, and it should be rapidly recognized during SARS-CoV-2 infection.

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Section: Introductionmentioning

confidence: 99%

Severe Acute Kidney Injury in Critically Ill Patients with COVID-19 Admitted to ICU: Incidence, Risk Factors, and Outcomes

Ghosn

Attallah

Badr³

et al. 2021

JCM

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“…The role of SARS-CoV-2 induced excessive inflammatory responses as a factor contributing to disease severity as a major outcome needs to be critically examined. Acute kidney injury (AKI), cardiac damage and abdominal pain are the most commonly reported co-morbidities of COVID-19 (3,4). SARS-CoV-2 infection may associate with damage occurring due to specific pathogenic conditions, including cytokine release syndrome (5).…”

Section: F O R P E E R R E V I E W D O N O T D I S T R I B U T E D E S T R O Y a F T E R U S E F O R P E E R R E V I E W D O N O T D mentioning

confidence: 99%

SARS-CoV-2 spike protein expressing epithelial cells promotes senescence associated secretory phenotype in endothelial cells and increased inflammatory response

Meyer

Patra

Mahantesh

et al. 2021

Preprint

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Increased mortality in COVID-19 often associates with thrombotic and microvascular complications. We have recently shown that SARS-CoV-2 spike protein promotes inflammatory cytokine IL-6/IL-6R induced trans-signaling responses which modulate MCP-1 expression in human endothelial cells. MCP-1 is secreted as a major component of the senescence associated secretory phenotype (SASP). Virus infected or Spike transfected human pulmonary epithelial cells (A549) exhibited an increase in senescence related marker proteins. TMNK; as a representative human endothelial cell line, when exposed to cell culture supernatant derived from A549 cells expressing SARS-CoV-2 spike protein (Spike CM) exhibited a senescence phenotype with enhanced p16, p21, and SA-β-galactosidase expression. Inhibition of IL-6 trans-signaling by Tocilizumab, prior to exposure of supernatant to endothelial cells, inhibited p16 and p21 induction. Likewise, inhibition of receptor signaling by Zanabrutinib or Brd4 function by AZD5153 also led to limited induction of p16 expression. Senescence lead to an enhanced level of adhesion molecule, ICAM-1 and VCAM-1 in human endothelial cells, and TPH1 attachment by in vitro assay. Inhibition of senescence or SASP function prevented ICAM/VCAM expression and leukocyte attachment. We also observed an increase in oxidative stress in A549 spike transfected and endothelial cells exposed to Spike CM. ROS generation in TMNK was reduced after treatment with the IL-6 specific inhibitor Tociliximab, and with the specific inhibitors Zanabrutinib and AZD5153. Taken together, we identified that the exposure of human endothelial cells to cell culture supernatant derived from SARS-CoV-2 spike protein expression displayed cellular senescence markers leading to enhanced leukocyte adhesion with coronary blockade potential.

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“…According to John Hopkins Coronavirus Resource Center, it has been responsible for more than 2 million deaths as of the 16 March 2021 [1]. Patients diagnosed with COVID-19 present a wide range of various impairments and organ dysfunctions, while the course of the disease depends on the individual, ranging from asymptomatic infection to severe symptoms and even fatal incidents [2,3]. The most common clinical manifestations include interstitial and alveolar pneumonia, with around 5-20% progressing to acute respiratory distress syndrome (ARDS), septic shock, or multiple organ failure [3][4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Pathophysiology and Clinical Manifestations of COVID-19-Related Acute Kidney Injury—The Current State of Knowledge and Future Perspectives

Smarz-Widelska¹,

Grywalska

Morawska

et al. 2021

IJMS

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The continually evolving severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic has resulted in a vast number of either acute or chronic medical impairments of a pathophysiology that is not yet fully understood. SARS-CoV-2 tropism for the organs is associated with bilateral organ cross-talks as well as targeted dysfunctions, among which acute kidney injury (AKI) seems to be highly prevalent in infected patients. The need for efficient management of COVID-related AKI patients is an aspect that is still being investigated by nephrologists; however, another reason for concern is a disturbingly high proportion of various types of kidney dysfunctions in patients who have recovered from COVID-19. Even though the clinical picture of AKI and COVID-related AKI seems to be quite similar, it must be considered that regarding the latter, little is known about both the optimal management and long-term consequences. These discrepancies raise an urgent need for further research aimed at evaluating the molecular mechanisms associated with SARS-CoV-2-induced kidney damage as well as standardized management of COVID-related AKI patients. The following review presents a comprehensive and most-recent insight into the pathophysiology, clinical manifestations, recommended patient management, treatment strategies, and post-mortem findings in patients with COVID-related AKI.

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Acute Kidney Injury in COVID-19: The Chinese Experience

Cited by 37 publications

References 93 publications

Severe Acute Kidney Injury in Critically Ill Patients with COVID-19 Admitted to ICU: Incidence, Risk Factors, and Outcomes

Severe Acute Kidney Injury in Critically Ill Patients with COVID-19 Admitted to ICU: Incidence, Risk Factors, and Outcomes

SARS-CoV-2 spike protein expressing epithelial cells promotes senescence associated secretory phenotype in endothelial cells and increased inflammatory response

Pathophysiology and Clinical Manifestations of COVID-19-Related Acute Kidney Injury—The Current State of Knowledge and Future Perspectives

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